Neurosensory Deficits After Myocardial Infarction · Neurosensory Deficits After Myocardial...

6
lnternational Tinnitus Journal, Vol.lO, No.l, 78-83 (2004) Neurosensory Deficits After Myocardial Infarction Gábor Bencze,1 Claus-Frenz Claussen,3 Lóránt Heid,1 Michael Kersebaum,3 Elemér Nagy,1 and Beáta Bencsik 2 I Central Military Hospital and 2Department of Otorhinolaryngology Head and Neck Surgery, Semmelweis University, Budapest, Hungary, and 3Neurootologisches Forschungsinstitut der 4-G-Forschung e. V., Bad Kissingen, Germany Abstract: Cardiovascular diseases are extremely widespread and often cause vestibular sys- tem dysfunctions. They are related mainly to organic lesions of the brain. To investigate neuro- otological functional changes, we compared two samples from among our patients, of whom those in group A (42 persons: 92.86% male, 7.14% female) had experienced myocardial in- farction within 1 year before our neurootometric investigation and those in group B had under- gone infarction 1 yearor more before examination (104 patients: 81.73% male, 18.27% female). Considering only the six most important vertigo symptoms experienced by patients, we found 1.48 symptoms per patient in group A and 2.02 symptoms per patient in group B. As regards acoustic symptoms, 45.24% of patients in group A experienced tinnitus and 52.38% reported hearing loss. ln patients in group B, 48.08% were affected with tinnitus and 58.65% with hear- ing loss. Abnormalities in the neurootometric measurements were revealed as follows: in group A, butterfly calorigrams, 80.95%; stepping-test craniocorpography (CCG), 64.29%; and bone conduction audiometry on the right side, 40.48%, and on the left side, 52.38%; in group B, butterfly calorigrams, 78.85%; stepping-test CCG, 61.54%; bone conduction audi- ometry on the right side, 28.85%, and on the left side, 41.35%. Key Words: craniocorpography; electronystagmography; hearing loss; myocardial infarc- tion; tinnitus; vertigo; vestibular dysfunction H uman brain consumes some 20-25% of the blood being pumped into the vessels by the heart. Thus, brain function also is affected when the heart does not work properly. As a result, pa- tients suffering from a heart attack or myocardial in- farction not only experience pain but later have other neurosensory symptoms from dysfunctions (e.g., in equi- Reprint reguests: Gábor Bencze, Eng., Central Military Hospital , Róbert-Károly krt. 44., H-1l34 Budapest, Hun- gary. Phone: 36-1-320-2418; Fax: 36-1-340-3129; E-mail: [email protected] This article is based on a lecture presented at the Thirtieth Annual Congress of the Neurootological and Equilibrio- metric Society, Porto, Portugal, April 3-5, 2003. This study was sponsored by Grant Projekt: D. 1417, through the LV A Baden-Württemberg, Stuttgart, Germany. 78 librium and hearing). People who survive a heart attack must undergo extensive rehabilitation, as a risk of a re- currence always remains. Therefore, we have chosen as an issue for this study a comparison between two post- myocardial infarction phases: (1) within 1 year, with patients still exhibiting existing complaints, and (2) more than 1 year after myocardial infarction. All 146 patients in this study underwent postinfarction rehabili- tation therapy. During the last 30 years, major data banks of pa- tients with neurootological complaints both in Würzburg at the Neurootological University Laboratories and in Bad Kissingen at the Neurootological Laboratories of the Forschungsinstitut der 4-G-Forschung have been built up. As a consequence, we were able to select two sam pIes of patients in whom we could compare the pa- tients' subjective complaints with the objective and quantitative findings in a thorough neurootological net- work analysis.

Transcript of Neurosensory Deficits After Myocardial Infarction · Neurosensory Deficits After Myocardial...

Page 1: Neurosensory Deficits After Myocardial Infarction · Neurosensory Deficits After Myocardial Infarction Gábor Bencze,1 Claus-Frenz Claussen,3 Lóránt Heid,1 Michael Kersebaum,3 Elemér

lnternational Tinnitus Journal, Vol.lO, No.l, 78-83 (2004)

Neurosensory Deficits After Myocardial Infarction

Gábor Bencze,1 Claus-Frenz Claussen,3 Lóránt Heid,1 Michael Kersebaum,3 Elemér Nagy,1 and Beáta Bencsik2

I Central Military Hospital and 2Department of Otorhinolaryngology Head and Neck Surgery, Semmelweis University, Budapest, Hungary, and 3Neurootologisches Forschungsinstitut der 4-G-Forschung e. V., Bad Kissingen, Germany

Abstract: Cardiovascular diseases are extremely widespread and often cause vestibular sys­tem dysfunctions. They are related mainly to organic lesions of the brain. To investigate neuro­otological functional changes, we compared two samples from among our patients, of whom those in group A (42 persons: 92.86% male, 7.14% female) had experienced myocardial in­farction within 1 year before our neurootometric investigation and those in group B had under­gone infarction 1 yearor more before examination (104 patients: 81.73% male, 18.27% female). Considering only the six most important vertigo symptoms experienced by patients, we found 1.48 symptoms per patient in group A and 2.02 symptoms per patient in group B. As regards acoustic symptoms, 45.24% of patients in group A experienced tinnitus and 52.38% reported hearing loss. ln patients in group B, 48.08% were affected with tinnitus and 58.65% with hear­ing loss. Abnormalities in the neurootometric measurements were revealed as follows: in group A, butterfly calorigrams, 80.95%; stepping-test craniocorpography (CCG), 64.29%; and bone conduction audiometry on the right side, 40.48%, and on the left side, 52.38%; in group B, butterfly calorigrams, 78.85%; stepping-test CCG, 61.54%; bone conduction audi­ometry on the right side, 28.85%, and on the left side, 41.35%.

Key Words: craniocorpography; electronystagmography; hearing loss; myocardial infarc­tion; tinnitus; vertigo; vestibular dysfunction

H uman brain consumes some 20-25% of the blood being pumped into the vessels by the heart. Thus, brain function also is affected

when the heart does not work properly. As a result, pa­tients suffering from a heart attack or myocardial in­farction not only experience pain but later have other neurosensory symptoms from dysfunctions (e.g., in equi-

Reprint reguests: Gábor Bencze, Eng., Central Military Hospital , Róbert-Károly krt. 44., H-1l34 Budapest, Hun­gary. Phone: 36-1-320-2418; Fax: 36-1-340-3129; E-mail: [email protected]

This article is based on a lecture presented at the Thirtieth Annual Congress of the Neurootological and Equilibrio­metric Society, Porto, Portugal, April 3-5, 2003. This study was sponsored by Grant Projekt: D. 1417, through the LV A Baden-Württemberg, Stuttgart, Germany.

78

librium and hearing). People who survive a heart attack must undergo extensive rehabilitation, as a risk of a re­currence always remains. Therefore, we have chosen as an issue for this study a comparison between two post­myocardial infarction phases: (1) within 1 year, with patients still exhibiting existing complaints, and (2) more than 1 year after myocardial infarction. All 146 patients in this study underwent postinfarction rehabili­tation therapy.

During the last 30 years, major data banks of pa­tients with neurootological complaints both in Würzburg at the Neurootological University Laboratories and in Bad Kissingen at the Neurootological Laboratories of the Forschungsinstitut der 4-G-Forschung have been built up. As a consequence, we were able to select two sam pIes of patients in whom we could compare the pa­tients' subjective complaints with the objective and quantitative findings in a thorough neurootological net­work analysis.

Page 2: Neurosensory Deficits After Myocardial Infarction · Neurosensory Deficits After Myocardial Infarction Gábor Bencze,1 Claus-Frenz Claussen,3 Lóránt Heid,1 Michael Kersebaum,3 Elemér

Neurosensory Deficits After Myocardial Infarction

PATIENTS AND METHODS

We chose our two sample groups of neurootological patients according to their medical histories: One group consisted of patients who reported experiencing a myo­cardial infarction within a year prior to our neurooto­metric investigation (N = 42), and a second group of patients who had experienced a myocardial infarction a year or more prior to our investigation (N = 104).

From ali 146 patients, we recorded a thorough neuro­otological history using the Neurootological Data Eval­uation-Claussen (NODEC) system. This systematic questionnaire contains sections for describing vertigo, nausea, hearing disorders, visual disorders, taste and smell disorders, neurological disorders, and other patho­logical mechanisms (e .g., trauma, cardiovascular dis­eases, kidney diseases, and diabetes mellitus). All pa­tients were also questioned about any drug treatment and about the use of negative substances (e.g. , smoking or drinking habits). A selected number of parameters appear in this article, as the entire body of data is too lengthy to include.

The practice of neurootology includes a large con­sideration of equilibriometry. From the field of equilib­riometry, we applied several tests to all our patients, in­cluding polygraphic electronystagmography (ENG) with a five-channel derivation of the patients' ENGs when being investigated for spontaneous nystagmus or experimentally provoked nystagmus. Simultaneously, in all patients a three-channel extremity derivation of electrocardiography (ECG) was recorded, giving us in­formation about the ongoing vegetative reactions dur­ing the test (see earlier).

Vestibuloocular tests being recorded by means of the five-channel ENG were monaural caloric tests, with 20 mI of 30° or 44°C water syringed over 30 seconds . The test results were evaluated by means of the Claus­sen butterfly chart.

The binaural vestibuloocular test was performed on the electronically programmable rotatory chair with a perrotatory supraminimal stimulus and a postrotatory supramaximal stimulus. The polygraphic ENGs were evaluated by means of the L-chart of the rotatory inten­sity damping test.

If the supraminimal monaural caloric warm re­sponse is considered the response to a weaker stimulus and the perrotatory nystagmus response on the rotatory intensity damping test is considered to be the stronger stimulus, a vestibular stimulus response intensity com­parison (VESRIC) can be established according to the balancing mechanisms within the equilibrium pathways in the central nervous system. By means of VESRIC, responses of a parallel behavior from recruitment phenomena and from decruitment phenomena can be differentiated.

lnternational Tinnitus Journal, Vol.IO, No. I, 2004

Regular retinoocular testing was performed by means of an ocular tracking test and by an optokinetic nystag­mus test. The results of these tests, however, had to be left out of this article owing to limits of publication space.

For investigating the vestibulospinal pathways , cranio­corpography (CCG) was used to record the head and trunk movements in space during standing and step­ping. The CCG patterns appear as a radar image of the trails of a human floating through space.

We analyzed hearing function by means of several audiometric tests. The hearing pathways first were in­vestigated by pure-tone threshold audiometry and by determining the discomfort threshold for estimating the acoustic dynamics. Social hearing function was mea­sured by speech audiometry, which also was used espe­cially for the statistics in this study. Tinnitus was masked according to its frequency and intensity .

Further hearing pathway investigations included tran­siently evoked otoacoustic emissions (TEOAE) , acoustic brainstem evoked potentials, and acoustic late or cortical evoked potentials (ALEP) . Ali the data assembled in this study were compiled into a spreadsheet (Microsoft's Excel). On this data bank, our data processing, statistic evaluations, and chart plotting have been performed.

RESULTS

This article focuses on the comparison of neurootologi­cal complaints among patients within I year after a myo­cardial infarction (group A) and those within a phase longer than 1 year after a myocardial infarction (group B). The samples contained 42 persons for group A and 104 persons for group B (total, 146 patients). As regards our statistics, we have complete individual descriptions within the patient files . AIso , a neurootological data bank, NODEC, has been established that comprises a list and a statistical analysis of the entire sample of 146 patients (Table 1) . We found among our patients who had experienced a myocardial infarction a variety of symptoms, which occurred with differing frequency among the groups (Table 2). The results ofthe vestibulo­ocular pathway test are presented in Table 3 .

For a synoptical overview of the most frequent com­bination of caloric responses , ali the butterfly patterns were transcribed by trinary code and thereafter statis­tically evaluated for both samples (groups A and B; Fig. 1) . From comparisons of the ipsidirectional vestib­uloocular responses due to monaural (caloric) and bin­aural (perrotatory) stimuli, we derived the VESRIC; the most frequent trinary-coded VESRIC patterns are Iisted in Figure 2. The figure reveals that the vestibuloocular nystagmus function is normal in patients in group A (UA =

16.67%) and in group B (us = 17.31%; see Fig. 2).

79

Page 3: Neurosensory Deficits After Myocardial Infarction · Neurosensory Deficits After Myocardial Infarction Gábor Bencze,1 Claus-Frenz Claussen,3 Lóránt Heid,1 Michael Kersebaum,3 Elemér

International Tinnitus Journal, Vol.IO, No. 1, 2004 Bencze et aI.

Table 1. Biographical Data of 146 Patients with Neurootological Complaints After Myocardial Infarction

Age (yr)

M F n (%) n (%) Mean SD

MI < I yr (n = 42) 39 (92.85) 3 (7.15) 53.54 8.77 MI > 1 yr(n = 104) 85 (81.73) 19 (18.27) 58.67 9.85 Total (n = 146) 124 (84.93) 22 (15.07)

BP = blood pressure; SD = standard deviation.

Table 2. Symptom Frequencies Noted in Post-Myocardial lnfarction Patients in Both Groups

GroupA Group B Patients Patients

Symptom (%) (%)

Vestibular symptoms Rocking 40.48 53.85 Lifting 7.14 3.85 Rotating 23.81 36.54 Falling 7.14 31.73 Blackout 38.10 36.54 Instability 30.95 39.42

Vegetative or nausea symptoms Sweating 40.48 53.85 Malaise 23.81 29.81 Retching 2.36 3.85 Vomitus 2.38 8.65 Collapse 19.05 12.50

Duration of single vertigo attacks Seconds 38.10 50.00 Minutes 35.71 32.69 Hoors 2.38 12.50 Days O 2.88

Visual disturbances Loss of acuity 69.05 75.00 Double vision 4.76 3.85 Oscillopsia I 2.38 8.65 Oscillopsia, jerking O 0.96 Amaurosis O 3.85 Oscillopsia II 16.67 25.96

Hearing symptoms Tinnitus 45.42 48.08 Hearing loss 52.38 58.65 Deafness 7.14 7.69 Ear sorgery 7.14 4.81 Humming sound O 1.92 Whistling sound 4.76 4.81 Noise trauma 9.52 5.77

Cardiovascular background disorders Hypertension 2 1.43 20.19 Hypotension 23.81 26.92 Arteriosclerosis 4.76 0.96 Myocardial infarction 64.29 74.04

oS 1 year previous to investigation 100 3.85 > I year previous to investigation 9.52 100

The vestibulospinal tests that were recorded and eval­uated by means of CCG are displayed in Figure 3. Typi­cal findings are underlined by graphic representations.

Some cases represent the individual pattems of the

80

Height Weight Systolic BP Diastolic BP (cm) (kg) (mm Hg) (mm Hg)

Mean SD Mean SD Mean SD Mean SD

172.65 7.66 77.41 9.76 143.75 14.93 85.00 5.77 170.15 7.50 74.44 10.79 134.50 17.39 81.66 7.90

Table 3. Statistical Evaluation of the Vestibuloocular Caloric Test with Electronystagmography (ENG) and Electrocardiography (ECG) Recording of 146 Patients with Neurootological Complaints After Myocardial Infarction

Myocardial Myocardial Infarction Infarction

< 1 yr 2: ] yr (n = 42) (n = 104)

Mean SD Mean SD

Caloric test (frequencies in Hz) Sp. nystagmus right 0.43 0.29 0.45 0.41 Sp. nystagmus left 0.45 0.34 0.38 0.31 44°C right 1.2 0.66 1.22 0.65 30°C right 1.34 0.66 1.38 0.75 44°C left 1.29 0.6 1.23 0.62 30°C left 1.42 0.72 1.46 0.79

ECO/min Sp. ECO 74.83 10.33 73.75 15.14 44°C right 74.31 9.58 71.71 14.95 44°C left 74.08 9.62 71.67 14.64 30°C right 74.71 9.41 72.01 14.82 30°C left 74.2 9.7 71.73 14.71

RlDT ECO rate, sitting position 73.23 10.7 68.13 13.28 Perrotatory ECO left 73.13 10.68 68.97 12.57 Perrotatory ECO right 71.08 11.31 68.52 12.74 Postrotatory ECO right 73.00 12.6 68.0 12.31 Postrotatory ECO left 71.71 11.52 68.97 1.57

RIDT = rotatory intesity-damping test; Sp. = spontaneous.

CCGs. Among the CCGs, the stepping-test CCG was clinically the most important for detecting pathology within the vestibulospinal pathways. Of the possible 81 pattems in trinary coding, the 12 most frequent are ranked in Figure 3 for groups A and B. Whereas group A shows only 35.71 % normal responses, this increases to 38.46% in group B. Only 5 of 12 pattems match for both the groups, of which pattem "s0200," expressing apure cerebello-ponto-medullary brainstem disinhibi­tion, is the most frequent single pattem-14.29% in group A and 7.69% in group B.

The audiometric results of the social hearing effi­cacy test by means of speech audiometry are Jisted in Table 4. Speech audiometry was evaluated according

Page 4: Neurosensory Deficits After Myocardial Infarction · Neurosensory Deficits After Myocardial Infarction Gábor Bencze,1 Claus-Frenz Claussen,3 Lóránt Heid,1 Michael Kersebaum,3 Elemér

Neurosensory Deficits After Myocardiallnfarction lnternational Tinnitus lournal, Vol.IO, No. 1, 2004

2 ,1p

-

I L

,7 ,7

6 , 6 81 81 6 " 8 SE

8 r- 81 ,,8 ,8 28

I-- I-- Iii 1m: • • IIIl • • I-- I--Iii • • '-

sOC(JO s0111 s2000 s1111 s0C(l2 30200 $2202 s0020 s0110 81000 $0022 $1011 $1110 92222 81100 $0222 82002 81010

Figure 1. Caloric butterfly test results (%) sorted according to the occurrences of the 12 most frequent patterns , which can be graphed or expressed by trinary coding (O = normal ; 1 = inhibited; 2 = disinhibited) with four digits (position I = right warm; position II = right cold; po­sition III = left warm; position IV = left cold). (Light bars = group A, or R I, :S I year post-myocardial infarction [N =

42];darkbars = groupB,orR2,>1 year post- myocardial infarction [N = 104].)

to the three important parameters-recognition of num­bers and words and loss of discrimination - for the right ear in 146 patients (groups A and group B) suffering from a myocardial infarction. The parameters were sta­tistically evaluated with respect to mean and standard deviation.

1 3 ,,,,

81 28

r- i 3 38 2

I .. ... I I. I-- III II III r- IR iii! I iii! '--

2

DISCUSSION It was the aim of this study to elucidate that patients after a myocardial infarction suffer from more than chest pain and reduction of their daily activities owing to restricted b100d fIow, the experience of shortness of breath, especially during exercise, and tightening pain

2 88 3 2 8

'''' ii ~i • 1 2 192 1 2 1, 2 ! II • • • • !1i\2

-- -- -- --

Figure 2. Dynamic vestibular stimulus response intensity comparison (VESRIC) sorted according to the occurrences of the 12 most frequent patterns. Combining the perrotatory part of the rotatory intensity-damping test with the caloric warm response , we can establish the so-called vestibular stimulus response intensity comparison (VESRIC). When combining the two-right-beating nystagmus and the left-beating nystagmus-we arrive at the charts of VESRIC, which can be graphed or expressed in trinary coding (O = normal ; I = inhibited; 2 = disinhibited) as four digits (position I = right warm; position II = pen'otatory right; position III = left warm; position IV = perrotatory left) . The test results can be categorized into three groups, in each of which are three subdivi­sions. The first group contains the parallel behavior, the second group contains the so-called recruiting phenomena, and within the third group are the so-called decruitment phenomena of VESRIC. (Light bars = group A, or RI, :S I year post-myocardial infarc­lion [N = 42]; dark bars = group B, or R2, > 1 year post-myocardial infarction [N = 104] .)

81

Page 5: Neurosensory Deficits After Myocardial Infarction · Neurosensory Deficits After Myocardial Infarction Gábor Bencze,1 Claus-Frenz Claussen,3 Lóránt Heid,1 Michael Kersebaum,3 Elemér

lnternational Tinnitus Journal, VoI.IO, No. I, 2004

Figure 3. Stepping-test craniocorpog­raphy results sorted according to the occurrences of the 12 most frequent patterns , which can be graphed or ex­pressed by trinary coding (O = normal; 1 = inhibited; 2 = disinhibited) with four digits (position I = displacement; I position II = lateral sway; position III = =II angular deviation; position IV = body :II

B e neze et aI.

spin). (Light bars = group A, or RI; ",'" ",'" ",'" ",'\o '\0'\0 ",'" ...... ",'" [1,'" [1,'\0 ",'\o ...... ...'" ",'" ",'" ...... ~ ",'\o '\0'\0 dark bars = group B, or R2.) ",,,,,,, ","''V ", ... '" ",,,,,,, ",,,,'" .,'\0'" ",,,,,,, ",,,,'> ",f' ",,,,,,, ","''V ",'\0'\0 ",,,,,,, ",'\o'" ",,,," ",'\o'" .,,,,'" .,'\0" .,'\0'\0

in the chest, known as angina pectoris. The study also exhibits a wider spectrum of complaints in such pa­tients' neurosensory system, as proved by special his­tory data (NODEC) and by the patients' equilibriomet­ric and audiometric findings (as described).

With respect to pathological anatomy, infarction is an area of coagulation necrosis in heart tissue due to local ischemia resulting from obstruction of circulation to the area, most commonly by a thrombus or embolus. Myocardial infarction is a gross necrosis of the myocar­dium, as a result of interruption of the blood supply to the area, as in coronary thrombosis. Myocardial infarc­tion may occur when coronary vessels are narrowed or occluded, such that the blood supply to the infarcted heart muscle is seriously impaired.

Congestive heart failure, arrhythmias, aortic or mi­traI stenosis , carotid hypersensitivity, and other vascu­lar lesions are frequently associated with vertigo or syncopal attacks (or both). Many patients report typical

Table 4. Statistical Evaluation of Speech Audiometry in 146 Patients with Neurootological Complaints After Myocardial Infarction

Speech audiometry , right Numbers Words Loss of discrimination

Speech audiometry, left Numbers Words Loss of discrimination

SO = standard deviation.

82

Myocardial Infarction

< 1 yr

Mean SD

20.12 32.52 69.72 16.16 14.88 33 .93

12.04 12.51 70.16 15.66

2.04 7.72

Myocardial Infarction

2:1 yr

Mean SD

23.87 26.25 75.22 20.19 11.27 25.46

25.03 25.02 76.94 20.33 12.62 25.74

syncopal attacks as giddiness. A syncopal attack must be careful1y distinguished from a vertiginous attack by a patient's medical history. Functionally, this is achieved by ECG, which we have performed for more than three decades in our neurootological laboratories in Würzburg and Bad Kissingen.

Syncope is an episodic loss of consciousness caused by vascular insufficiency in the brain. Its management is distinctly different from that of vertigo. Hypoperfu­sion of the brain, characterized by unconsciousness or by light-headedness, diminished vision, or blackouts, is indicative of a syncope. Conversely, a sensation of mo­tion without external stimuli or a sensation of spinning, whirling, swaying, staggering or, simply , unsteadiness or instability is indicative of vertigo, which now can be verified by ENG, ECG, and CCG. Sometimes, how­ever, typical features of a syncope may be associated with vertiginous symptoms along with central nervous system disorders (e.g ., diplopia, dysarthria, focal sen­sorimotor disturbance , and occipital headache) . This unusual combination of features suggests the rare pos­sibility of syncopal attack (ischemia) of the posterior cerebral circulation .

Cardiovascular diseases are extremely widespread and often cause vestibular system dysfunctions. They can be related also to resulting organic lesions of the brain . Vertigo has been shown to occur mainly in pa­tients with disturbances in circulation in the verte­brobasilar blood supply and may be evaluated objec­tively by various types of vestibular deficiencies (i.e., peripheral or central or both). The cause of vestibular disorders appears to be a vasomotor disturbance mainly in the vertebrobasilar system . A certain correlation is seen between different varieties of nystagmus and a rate of vestibular asymmetry in persons suffering from vertigo due to cardiovascular pathology.

As far as the cardiovascular system is concerned, some researchers question whether individuais with

Page 6: Neurosensory Deficits After Myocardial Infarction · Neurosensory Deficits After Myocardial Infarction Gábor Bencze,1 Claus-Frenz Claussen,3 Lóránt Heid,1 Michael Kersebaum,3 Elemér

Neurosensory Deficits After MyocardialInfarction

cardiovascular diseases are prone to develop sensori­neural deafness. Hearing impairment parallels the inci­dence of coronary heart disease; however, not all car­diac patients develop hearing loss. This could be owing to biological variability from one individual to the other; that is , this phenomenon is likely to have a more com­pIe x genetic background. Attacks of vertigo, dizziness , giddiness, blackout, instability , rocking more than ro­tating, tinnitus , and transient hearing loss can also be considered as early symptoms of coronary insufficiency.

ln general, the number of pathological vestibular re­actions is much higher in patients who experience myo­cardial infarction than in patients in other stroke groups. The brain needs to be fed, and when the cardiac power is diminished (e.g., by myocardial infarction), we find various systems with vestibuloocular and vestib­ulospinal pathological functions, even in speech audi­ometry, increased discrimination loss , and pooling down of the threshold discrimination loss .

BIBLIOGRAPHY

Alexander G, Marburg O, Brunner H. Handbuch der Neurol­ogie des Ohres , Bd. II , l. Berlin: Urban & Schwartzen­berg,1928.

Bergmann J, Bertora G. Schwindel bei Herz-Kreislauf-Kranken. Proc NES 8:403- 410, 1981.

Bodo G. Connection between the vestibular and circulatory systems. Excerpta Medica 708:19-23,1986.

Claussen C-F. Schwindel-Symptomatik, Diagnostik, Therapie. Hamburg: Neu-Isenburg, 1981.

Claussen C-F. Presbyvertigo. Presbyataxie, Presbytinnitus. Berlin: Springer-Verlag, 1985 .

Claussen C-F, Aust G, Schafer W-D, von Schlachta L Atlas der Elektronystagrnographie. Hamburg: Werner Rudat, 1986.

Claussen C-F, Claussen E. Vertigo, Nausea, Tinnitus und Hy­poacusia in Cardiovascular Diseases. Excerpta Medica [lnternational Congress Seriesl 708:43-48, 1986.

International Tinnitlls JOllrnal, Vol.lO, No. 1,2004

Deeg P. Automatic data processing in cardiology. Proc NES 10:100-101,1983.

Deeg P. Differential diagnosis of cardiovascular vertigo. Ex­cerpta Medica 708:49-54,1988.

Deeg P, Claussen C-F. Schwindel und Nausea: Alarmzeichen gefahrlicher Herz-Kreislauf-Erkrankungen. DtschArzteb­latt 80:22, 1983.

Deeg P, Meyer-Spelbrink W, Schneider KW. Typische kardio­vasculsre Erkrankungen mit funktioneller Himstammbee­intrachtigung. GNA 1978:831-837.

Deeg P, Schneider KW, C1aussen C-F. Ober erne Myokardio­pathie mit Schwindel. GNA 1978:839-851.

Georgopoulos G, Kastanakis S, Petmezakis J, Askitis P. Sud­den transient sensorineural deafness: Sign of coronary in­sufficiency. Excerpta Medica 791 :265-268, 1988.

Grigoriev G.M. Vertigo and central dysequilibrium in patients with cardiovascular pathology. Proc NES 19(20):93-96, 1994.

Hart CW. ENG test data acquisition and reduction . Proc NES 10:195-201,1983.

Hoyer S, Weidner G, Breuer H. Exemplar functiones cerebri. Wiesbaden: Albert-Roussel- Phanna-GmbH, 1982.

Kobrak F. Die vascularen Erkrankungen des Labyrinths. ln: Handbuch der Neurologie des Ohres . Berlin: Urban & Schwartzenberg, 1928.

Meyer-Spelbrink W , Deeg P, Schneider KW, Claussen C-F. Typische Gleichgewichtsfunktionserkrankungen bei kardio­vascularen Storungen. GNA 1978:853-863.

Norre ME, Degroote M.lnfluence of caloric and rotation test­ing upon blood pressure and pulse rate. Excerpta Medica 791:139-142,1988.

Schneider KW. Kardiogen bedingte Schwindelerscheinun­gen. Proc NES 4:385-390,1975.

Schneider KW. Vestibularisfunktion bei Kardiovaskularen Erkrankungen. Proc NES 6(2):823-829,1978.

Stein C. Die Arteriosklerose des Gehsrorganes . Aus Hand­buch der Neurologie des Ohres. Berlin: Urban & Schwart­zenberg , 1928.

Stiefler G. Vaskulare Erkrankungen im Hirnstarnm und Kleinhirn. Aus Handbuch der Neurologie des Ohres. Ber­lin: Urban & Schwartzenberg, 1928.

83